1,157 results on '"Masatsugu Hori"'
Search Results
1152. 744-1 Endogenous Nitric Oxide Attenuates Myocardial Inotropic Responses in Ischemic Myocardium of the Canine Heart
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Koichi Node, Masatsugu Hori, Masafumi Kitakaze, Michihiko Tada, Takenobu Kamada, Hiroaki Kosaka, Michitoshi Inoue, Yuji Okuyama, Kazuo Komamura, and Hiroharu Funaya
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Inotrope ,medicine.medical_specialty ,Contraction (grammar) ,business.industry ,Vasodilation ,Blood flow ,Venous blood ,Anterior Descending Coronary Artery ,Nitric oxide ,chemistry.chemical_compound ,chemistry ,Internal medicine ,Anesthesia ,medicine ,Cardiology ,business ,Cardiology and Cardiovascular Medicine ,Perfusion - Abstract
Nitric oxide (NO) is reported to attenuate myocardial contraction, raising the possibility that endogenous NO decreases the inotropic response of ischemic myocardium. In 42 dogs, the left anterior descending coronary artery was perfused with blood from the left carotid artery. During reduction of perfusion pressure (1 03 ± 6 to 53 ± 4 mmHg) so that coronary blood flow (CBF) decreases to 60% of the control, fractional shortening (FS) of the perfused area decreased from 23.3 ± 3.3 to 8.4 ± 1.3%. Intravenous infusions of isoproterenol (ISO, 75 and 150 ng/kg/min) increased FS to 15.9 ± 33 and 22.5 ± 2.5%, respectively. An infusion of L-NAME, an inhibitor of NO synthase, did not alter FS in the non-ischemic condition (24.5 ± 2.1%). However, changes in FS due to reduction of C8F to 60% (FS:14.3 ± 1.3%), and intravenous infusions of ISO during coronary hypoperfusion (FS:23.3 ± 3.3 and 32.3 ± 2.8%) were augmented in the L-NAME group compared with the untreated group. Lactate extraction ratio (-4.1 ± 2.2 vs -15.6 ± 4.2%), and pH in the coronary venous blood (7.32 ± 0.03 vs 7.27 ± 0.03) in the L-NAME group were lower than the untreated group during coronary hypoperfusion. Furthermore, L-arginine restored metabolic dysfunction due to L-NAME in the ischemic myocardium. These results indicate that endogenous NO attenuates myocardial contractile function in the ischemic heart and improves myocardial metabolic function. NO and NO donors such as nitrates in the ischemic heart disease may play an importrant role for myocardial energysparing effect as well as coronary vasodilation.
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1153. Association Between the Connexin37 Polymorphism and Peripheral Arterial Disease in Subjects With Type 2 Diabetes
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NAOTO KATAKAMI, KEN'YA SAKAMOTO, HIDEAKI KANETO, MUNEHIDE MATSUHISA, IKKI SHIMIZU, FUKASHI ISHIBASHI, TAKESHI OSONOI, ATSUNORI KASHIWAGI, RYUZO KAWAMORI, MASATSUGU HORI, and YOSHIMITSU YAMASAKI
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- 2009
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1154. Oxidative stress and left ventricular remodelling after myocardial infarction.
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Masatsugu Hori and Kazuhiko Nishida
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OXIDATIVE stress , *VENTRICULAR remodeling , *OXYGEN in the body , *CELLULAR signal transduction , *CELL death , *CYTOKINES , *METALLOPROTEINASES - Abstract
In acute myocardial infarction (MI), reactive oxygen species (ROS) are generated in the ischaemic myocardium especially after reperfusion. ROS directly injure the cell membrane and cause cell death. However, ROS also stimulate signal transduction to elaborate inflammatory cytokines, e.g. tumour necrosis factor-α (TNF-α), interleukin (IL)-1β and -6, in the ischaemic region and surrounding myocardium as a host reaction. Inflammatory cytokines also regulate cell survival and cell death in the chain reaction with ROS. Both ROS and inflammatory cytokines are cardiodepressant mainly due to impairment of intracellular Ca2+ homeostasis. Inflammatory cytokines stimulate apoptosis through a TNF-α receptor/caspase pathway, whereas Ca2+ overload induced by extensive ROS generation causes necrosis through enhanced permeability of the mitochondrial membrane (mitochondrial permeability transition). Apoptosis signal-regulating kinase-1 (ASK1) is an ROS-sensitive, mitogen-activated protein kinase kinase kinase that is activated by many stress signals and can activate nuclear factor κB and other transcription factors. ASK1-deficient mice demonstrate that the ROS/ASK1 pathway is involved in necrotic as well as apoptotic cell death, indicating that ASK1 may be a therapeutic target to reduce left ventricular (LV) remodelling after MI. ROS and inflammatory cytokines activate matrix metalloproteinases which degrade extracellular matrix, causing a slippage of myofibrils and hence LV dilatation. Consequently, collagen deposition is increased and tissue repair is enhanced with myocardial fibrosis and angiogenesis. Since the extent of LV remodelling is a major predictor of prognosis of the patients with MI, the therapeutic approach to attenuating LV remodelling is critically important. [ABSTRACT FROM AUTHOR]
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- 2009
1155. Risedronate, an effective treatment for glucocorticoid-induced bone loss in CKD patients with or without concomitant active vitamin D (PRIUS-CKD).
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Naohiko Fujii, Takayuki Hamano, Satoshi Mikami, Yasuyuki Nagasawa, Yoshitaka Isaka, Toshiki Moriyama, Masaru Horio, Enyu Imai, Masatsugu Hori, and Takahito Ito
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KIDNEY diseases ,VITAMIN D ,GLUCOCORTICOIDS ,ADRENOCORTICAL hormones - Abstract
Background. Recent post hoc analysis proved the efficacy and tolerability of risedronate in osteoporotic patients with renal impairment, but the combination of active vitamin D in chronic kidney disease (CKD) patients taking glucocorticoids remains unknown. Methods. We conducted a prospective study enroling 114 CKD patients (creatinine clearance â¥30âml/min/1.73âm2) receiving glucocorticoid therapy for â¥6 months. Eighty-eight subjects who had received active vitamin D (aVD) were randomly assigned to either a group treated with aVD only (group A), or to a group also receiving risedronate 2.5âmg/day (group B). The remaining patients (group C) received risedronate only. Results. After 1 year 100 subjects were analysed. Risedronate was effective on the lumbar spine, but not on the femoral neck. The lumbar bone mineral density (BMD) significantly increased by 2.8 and 2.5% in groups B and C, respectively, but decreased by 1.0% in group A. Serum N-terminal telopeptides of type I collagen (S-NTX) and bone alkaline phosphatase (ALP) fell significantly in groups B and C at 3 and 6 months, respectively, while in group A S-NTX remained unchanged and bone ALP significantly increased. There was no significant difference between groups B and C regarding BMD and bone markers. The reduction rate of S-NTX (bone ALP) at 6 months predicted the increase in lumbar BMD at 1 year with a sensitivity of 73% (34%) and a specificity of 46.2% (100%). Conclusions. Risedronate is effective in increasing BMD with or without aVD in CKD patients receiving long-term glucocorticoid therapy. Bone markers are of some use in predicting the response to anti-resorptive therapy. [ABSTRACT FROM AUTHOR]
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- 2007
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1156. Ca2+/calmodulin-dependent protein kinase II activates apoptosis signal-regulating kinase 1 and nuclear factor-kappaB to induce cardiomyocyte hypertrophy
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Kazunori, Kashiwase, Kinya, Otsu, Osamu, Yamaguchi, Syungo, Hikoso, Toshihiro, Takeda, Tetsuya, Watanabe, Masayuki, Taniike, Michio, Asahi, Kazuhiko, Nishida, and Masatsugu, Hori
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Ca2+/calmodulin-dependent protein kinase (CaMK) is an important molecule in cardiomyocyte hypertrophy. We previously showed that the activation of apoptosis signal-regulating kinase 1 (ASK1) or its transcription factor NF-kappaB is sufficient for cardiomyocyte hypertrophy. Recently, it was reported that in C. elegans, UNC-43, a homologue to CaMKII, activates NSY-1, which is a homologue of mammalian ASK1. We hypothesized that ASK1-NF-kappaB signaling pathway was a downstream target of CaMKII. In vitro kinase assay indicates that infection of isolated neonatal cardiomyocytes with adenoviral vector expressing CaMKIIdelta3 (AdCaMKIIdelta3) induced the activation of ASK1, while KN93, an inhibitor of CaMKII, inhibited phenylephrine-induced ASK1 activation. Overexpression of CaMKIIdelta3 induced hypertrophic responses, including increases in protein synthesis, atrial natriuretic factor production and the enhancement of sarcomeric organization. KN93 inhibited these hypertrophic responses induced by phenylephrine. Infection of cardiomyocytes with an adenoviral vector expressing a dominant negative mutant of ASK1 (AdASK(KM)) inhibited the CaMKIIdelta3-induced hypertrophic responses. To evaluate NF-kappaB activation, we measured the activity of kappaB-dependent reporter gene assay and IkappaBalfa degradation by Western blotting. Overexpression of CaMKIIdelta3 increased the luciferase activity and induced IkappaBalfa degradation. Coinfection of AdCaMKIIdelta3 with AdASK (KM) and preincubation with KN93 attenuated CaMKIIdelta3- and phenylephrine-induced NF-kappaB activation, respectively. Expression of a degradation resistant mutant of IkappaBalfa inhibited CaMKIIdelta3-induced hypertrophic responses. These results indicate that CaMKIIdelta3 induces cardiomyocyte hypertrophy mediated through ASK1-NF-kappaB signal transduction pathway.
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- 2004
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1157. Rivaroxaban with or without aspirin in patients with stable coronary artery disease: an international, randomised, double-blind, placebo-controlled trial.
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Connolly, Stuart J., Eikelboom, John W., Bosch, Jackie, Dagenais, Gilles, Dyal, Leanne, Lanas, Fernando, Metsarinne, Kaj, O'Donnell, Martin, Dans, Anthony L., Jong-Won Ha, Parkhomenko, Alexandr N., Avezum, Alvaro A., Lonn, Eva, Liu Lisheng, Torp-Pedersen, Christian, Widimsky, Petr, Maggioni, Aldo P., Felix, Camilo, Keltai, Katalin, and Masatsugu Hori
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CORONARY disease , *RIVAROXABAN , *ASPIRIN , *MYOCARDIAL infarction , *HEMORRHAGE , *PATIENTS , *THERAPEUTICS , *CARDIOVASCULAR disease prevention , *STROKE prevention , *ANTICOAGULANTS , *COMBINATION drug therapy , *COMPARATIVE studies , *DISEASES , *DRUG administration , *DOSE-effect relationship in pharmacology , *RESEARCH methodology , *MEDICAL cooperation , *RESEARCH , *STROKE , *EVALUATION research , *RANDOMIZED controlled trials , *BLIND experiment , *PLATELET aggregation inhibitors , *PREVENTION ,CARDIOVASCULAR disease related mortality - Abstract
Background: Coronary artery disease is a major cause of morbidity and mortality worldwide, and is a consequence of acute thrombotic events involving activation of platelets and coagulation proteins. Factor Xa inhibitors and aspirin each reduce thrombotic events but have not yet been tested in combination or against each other in patients with stable coronary artery disease.Methods: In this multicentre, double-blind, randomised, placebo-controlled, outpatient trial, patients with stable coronary artery disease or peripheral artery disease were recruited at 602 hospitals, clinics, or community centres in 33 countries. This paper reports on patients with coronary artery disease. Eligible patients with coronary artery disease had to have had a myocardial infarction in the past 20 years, multi-vessel coronary artery disease, history of stable or unstable angina, previous multi-vessel percutaneous coronary intervention, or previous multi-vessel coronary artery bypass graft surgery. After a 30-day run in period, patients were randomly assigned (1:1:1) to receive rivaroxaban (2·5 mg orally twice a day) plus aspirin (100 mg once a day), rivaroxaban alone (5 mg orally twice a day), or aspirin alone (100 mg orally once a day). Randomisation was computer generated. Each treatment group was double dummy, and the patients, investigators, and central study staff were masked to treatment allocation. The primary outcome of the COMPASS trial was the occurrence of myocardial infarction, stroke, or cardiovascular death. This trial is registered with ClinicalTrials.gov, number NCT01776424, and is closed to new participants.Findings: Between March 12, 2013, and May 10, 2016, 27 395 patients were enrolled to the COMPASS trial, of whom 24 824 patients had stable coronary artery disease from 558 centres. The combination of rivaroxaban plus aspirin reduced the primary outcome more than aspirin alone (347 [4%] of 8313 vs 460 [6%] of 8261; hazard ratio [HR] 0·74, 95% CI 0·65-0·86, p<0·0001). By comparison, treatment with rivaroxaban alone did not significantly improve the primary outcome when compared with treatment with aspirin alone (411 [5%] of 8250 vs 460 [6%] of 8261; HR 0·89, 95% CI 0·78-1·02, p=0·094). Combined rivaroxaban plus aspirin treatment resulted in more major bleeds than treatment with aspirin alone (263 [3%] of 8313 vs 158 [2%] of 8261; HR 1·66, 95% CI 1·37-2·03, p<0·0001), and similarly, more bleeds were seen in the rivaroxaban alone group than in the aspirin alone group (236 [3%] of 8250 vs 158 [2%] of 8261; HR 1·51, 95% CI 1·23-1·84, p<0·0001). The most common site of major bleeding was gastrointestinal, occurring in 130 [2%] patients who received combined rivaroxaban plus aspirin, in 84 [1%] patients who received rivaroxaban alone, and in 61 [1%] patients who received aspirin alone. Rivaroxaban plus aspirin reduced mortality when compared with aspirin alone (262 [3%] of 8313 vs 339 [4%] of 8261; HR 0·77, 95% CI 0·65-0·90, p=0·0012).Interpretation: In patients with stable coronary artery disease, addition of rivaroxaban to aspirin lowered major vascular events, but increased major bleeding. There was no significant increase in intracranial bleeding or other critical organ bleeding. There was also a significant net benefit in favour of rivaroxaban plus aspirin and deaths were reduced by 23%. Thus, addition of rivaroxaban to aspirin has the potential to substantially reduce morbidity and mortality from coronary artery disease worldwide.Funding: Bayer AG. [ABSTRACT FROM AUTHOR]- Published
- 2018
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